Cyclic Nucleotide-Gated Ion Channel 2 modulates auxin homeostasis and signaling

Cyclic Nucleotide Gated Ion Channels (CNGCs) have been firmly established as Ca²⁺-conducting ion channels that regulate a wide variety of physiological responses in plants. CNGC2 has been implicated in plant immunity and Ca²⁺signaling due to the autoimmune phenotypes exhibited by null mutants ofCNGC2. However,cngc2mutants display additional phenotypes that are unique among autoimmune mutants, suggesting that CNGC2 has functions beyond defense and generates distinct Ca²⁺signals in response to different triggers. In this study we found thatcngc2mutants showed reduced gravitropism, consistent with a defect in auxin signaling. This was mirrored in the diminished auxin response detected by the auxin reporters DR5::GUS and DII-VENUS and in a strongly impaired auxin-induced Ca²⁺response. Moreover, thecngc2mutant exhibits higher levels of the endogenous auxin indole-3-acetic acid (IAA), indicating that excess auxin incngc2causes its pleiotropic phenotypes. These auxin signaling defects and the autoimmunity syndrome ofcngc2could be suppressed by loss-of-function mutations in the auxin biosynthesis geneYUCCA6(YUC6), as determined by identification of thecngc2suppressor mutantrepressor of cngc2(rdd1) as an allele ofYUC6. A loss-of-function mutation in the upstream auxin biosynthesis geneTRYPTOPHAN AMINOTRANSFERASE OF ARABIDOPSIS(TAA1, WEAK ETHYLENE INSENSITIVE8) also suppressed thecngc2phenotypes, further supporting the tight relationship between CNGC2 and the TAA–YUC-dependent auxin biosynthesis pathway. Taking these results together, we propose that the Ca²⁺signal generated by CNGC2 is a part of the negative feedback regulation of auxin homeostasis in which CNGC2 balances cellular auxin perception by influencing auxin biosynthesis.